Influences of Estrogen Deficiency and Graded Reductions in Exercising Muscle Blood Flow on Arterial Blood Pressure Responses in Healthy Women
Open Access
- Author:
- Barrett, Megan Ann
- Graduate Program:
- Kinesiology
- Degree:
- Master of Science
- Document Type:
- Master Thesis
- Date of Defense:
- March 23, 2016
- Committee Members:
- David Nathan Proctor, Thesis Advisor/Co-Advisor
James Anthony Pawelczyk, Thesis Advisor/Co-Advisor
Mary Jane De Souza, Thesis Advisor/Co-Advisor - Keywords:
- estrogen
metaboreflex
postmenopausal
blood pressure - Abstract:
- Postmenopausal women have been shown to exhibit larger arterial blood pressure responses to exercise compared to premenopausal women, and age matched men. These findings, plus those documenting an attenuation of exercise blood pressure following estrogen replacement, are suggestive of a role for estrogen deficiency in mediating the exaggerated cardiovascular response. However, the mechanisms by which this augmented blood pressure response is achieved and estrogens contribution remains incompletely understood. As such, the objective of this thesis was to determine the effects of acute and chronic estrogen deficiency on the hemodynamic responses to rhythmic exercise with graded reductions in muscle blood flow. Seventeen healthy women participated in this study (7 postmenopausal women, 57-64 yrs; 10 premenopausal women, 20-28 yrs). To discern the effect of acute estrogen fluctuations on the cardiovascular responses to rhythmic exercise with progressive muscle ischemia, premenopausal women were tested at two different time points during their menstrual cycle; when estrogen levels were at their nadir (early follicular phase, days 2-6) and at their peak (late follicular phase). Hemodynamic responses in each subject were assessed (Finometer) at rest and during mild (10% MVC) rhythmic (30 contractions/min) handgrip exercise. Following a 4-minute free flow exercise period, a blood pressure cuff on the subject’s upper arm was progressively inflated at a rate of 20 mmHg/minute. Subjects continued to exercise until volitional fatigue after which contractions ceased but the blood pressure cuff remained inflated (3 minutes) to isolate the contribution of the muscle metaboreflex. As expected, postmenopausal women generated greater systolic blood pressure response at fatigue (ΔSBP: 24.7±3.9 vs 39.4±3.6 mmHg) (p < 0.05), a response that tended to remain during the period of metaboreflex isolation that followed (ΔSBP: 17.6±3.1 vs 27.3±4.2 mmHg) (p = 0.07). Importantly, the pressor response generated at fatigue appeared to be mediated almost exclusively by a rise in peripheral resistance in the postmenopausal women (ΔTPR: 22.7±39.8 vs 218.7±61.1 dyn•s/cm5) (p < 0.05), while changes in cardiac output played a larger role in the premenopausal women (ΔQ̇: 1.8±0.5 vs 0.4±0.7 L/min). The differential nature of the cardiac output response between groups was mediated by differences in stroke volume (ΔSV: 10.6±4.3 vs -16.4±11.6 mL/beat) (p < 0.05), rather than heart rate. Additionally, at high relative arterial cuff pressures, when the muscle metaboreflex was engaged, the percent reduction in brachial blood flow across increasing cuff pressures was smaller in the postmenopausal than the premenopausal women, indicating that the elevated pressor response in the postmenopausal women appeared to confer a flow advantage. Acute estrogen deficiency appeared to some extent to mirror the findings noted with chronic estrogen changes. Specifically, although the pressor response to rhythmic exercise and during metaboreflex isolation were not different between the two menstrual phases, elevated estrogen levels appeared to shift the components of the pressor response to an increased reliance on stroke volume changes, both during exercise (ΔSV: 17.7±5.4 vs 10.6±4.3 mL/beat) (p < 0.05) and during the period of post exercise circulatory arrest that followed (ΔSV: 17.8±5.8 vs 11.8±4.6 mL/beat) (p < 0.05). Importantly, the divergent nature of the stroke volume response between menstrual phases was not present during the free flow exercise period or at low relative cuff pressures during progressive arterial occlusion suggesting a role for acute estrogen changes on the components of the metaboreflex-induced pressor response. In conclusion, the present study provides evidence for estrogenic effects on the hemodynamic responses to rhythmic exercise, particularly when the muscle metaboreflex is engaged.